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Biomedical subjects

J Puurunen

Publications and source records attributed to J Puurunen.

At least 37 records · Page 2Linked to original sources
PubMed1985

Role of putative neurotransmitters in the central gastric antisecretory effect of prostaglandin E2 in rats.

The role of putative neurotransmitters of the central nervous system in the central gastric antisecretory effect of prostaglandin E2 (PGE2) was investigated in pylorus-ligated rats. Pretreatment of the rats with an intracerebroventricular (i.c.v.) injection of 6-hydroxydopamine (6-OHDA) prevented the antisecretory effect of the i.c.v. administration of PGE2, whereas pretreatment with 5,6-dihydroxytryptamine (5,6-DHT) plus p-chlorophenylalanine (PCPA) had no effect. I.c.v.-administered phentolamine and idazoxan antagonized the inhibition of gastric secretion induced by i.c.v. PGE2, whereas prazosin, propranolol and sulpiride injected via the same route were ineffective. Diphenhydramine, cimetidine, naloxone and theophylline, all administered i.c.v., did not modify the antisecretory effect of i.c.v. PGE2. The results suggest that an activation of alpha 2-adrenoceptors in the brain is involved in the central gastric antisecretory effect of PGE2, whereas neither central 5-hydroxytryptamine receptors, alpha 1- or beta-adrenoceptors, D2-dopamine receptors, histamine or opioid receptors nor adenosine seem to play any role here.

5,6-Dihydroxytryptamine↗
PubMed1985

Peripheral cardiovascular alpha- and beta-adrenergic effects of some hypotensive and bradycardic arylalkyl imidazole derivatives in the rat.

In pithed rats, a series of four alkyl bridge analogues of 4(5)-substituted arylalkyl imidazole induced alpha-adrenoceptor-mediated vasoconstriction and inhibition of electrically stimulated tachycardia. These effects were induced in the order of potency clonidine = MPV 207 greater than MPV 295 greater than MPV 304 greater than MPV 390, correlating with the length of the alkyl bridge between the phenyl and imidazole moieties. The peripheral postsynaptic actions of MPV 207 and MPV 304 were attenuated by prazosin (0.1 mg kg-1 i.v.) and yohimbine (1 mg kg-1 i.v.). The pressor responses induced by MPV 295 were antagonized only by yohimbine (0.3 and 1 mg kg-1 i.v.). The peripheral sympathoinhibitory action of these compounds was antagonized by yohimbine (1 mg kg-1 i.v.). In spontaneously beating rat atria, the MPV compounds showed neither agonistic nor antagonistic activity at cardiac postsynaptic alpha- and beta-adrenoceptors. The results indicate that the hypotensive and bradycardic MPV compounds are agonists at peripheral cardiovascular alpha-adrenoceptors. The extension of the alkyl bridge between the phenyl and imidazole moieties reduces their activity at alpha-adrenoceptors. Finally, MPV 295 seems to be a selective agonist of peripheral alpha 2-adrenoceptors in the cardiovascular system of the pithed rat.

Animals↗
PubMed1984

Vagally mediated bradycardiac effect of prazosin in anaesthetized rats.

Prazosin at doses of 100 or 1000 nmol/kg i.v. induced bradycardia in urethane-anaesthetized rats. The bradycardia was completely abolished by atropine pretreatment or vagotomy. Prazosin also stimulated gastric acid secretion. This effect was completely abolished by vagotomy. The maximal hypotensive effect after prazosin i.c.v. occurred 10 min later than with i.v. administration. It is concluded that prazosin possesses vagal a stimulating property that may in part explain its modest tachycardiac effect seen in clinical use. The mechanism of vagal stimulation by prazosin remains unclear. The present findings suggest that prazosin does not exert any direct effects on central vagal structures accessible from the ventricular space.

Anesthesia↗
PubMed1984

Centrally administered PGE2 inhibits gastric secretion in the rat by releasing vasopressin.

The pituitary mechanism of the central inhibitory effect of PGE2 on gastric secretion was investigated in rats. The intravenous (i.v.) injection of neurointermediate lobe extracts but not of anterior lobe extracts inhibited gastric secretion in pylorus-ligated rats. The i.c.v. administration of 3 micrograms of PGE2 increased the plasma level of vasopressin but had no effect on plasma beta-endorphin/beta-lipotropin. The i.v. administration of 10 micrograms d(CH2)5Tyr(Me) AVP, a vasopressin antagonist, prevented the inhibition of gastric secretion induced by i.c.v. administration of 3 micrograms PGE2 to pylorus-ligated rats. The results indicate that the central antisecretory action of PGE2 is due to the release of vasopressin from the pituitary gland.

Animals↗
PubMed1984

Central gastric antisecretory action of prostaglandin E2: the involvement of the pituitary gland.

The mechanism of the gastric antisecretory action of intracerebroventricularly administered prostaglandin (PG)E2 was investigated in conscious, pylorus-ligated rats. It was found that intracerebroventricular administration of 3 micrograms of PGE2 inhibited carbachol-stimulated gastric secretion (acid, pepsin and volume) in vagotomized rats and spontaneous secretion in rats with intact vagi to the same degree. Hypophysectomy prevented the antisecretory effect of PGE2, whereas neither adrenalectomy nor gastric sympathectomy (extirpation of the ganglion coeliacum and mesentericus superius) did modify it. The results suggest that an altered pituitary activity, but not the autonomic nervous system, is involved in the mechanism mediating PGE2-induced inhibitory impulses from the brain on gastric secretion.

Adrenalectomy↗
PubMed1983

Central inhibitory action of prostaglandin E2 on gastric secretion in the rat.

The central nervous system action of prostaglandin E2 (PGE2) on gastric secretion was studied in conscious pylorus-ligated rats. It was found that 1-10 micrograms of PGE2 given i.c.v. reduced the gastric output of acid, pepsin and fluid in a dose-dependent manner whereas 30-300 micrograms was required for inhibition when given subcutaneously. Given i.c.v. 400 micrograms of indomethacin, a potent inhibitor of prostaglandin biosynthesis, enhanced gastric secretion but not when given intramuscularly. It is concluded that PGE2 has a central inhibitory action on gastric secretion in conscious rats. In addition, the possibility that PGE2 may be involved as inhibitory modulator in the central control of gastric secretion warrants further attention.

Animals↗
PubMed1983

Combined ulcerogenic effect of ethanol and acetylsalicylic acid on the gastric mucosa of the rat.

The effect on rat gastric mucosa of ethanol and acetylsalicylic acid given at two doses singly or in combination were studied by administering the drugs into the stomach. 40% ethanol alone caused many ulcerations after 5 h, and the effect was even more marked with simultaneous administration of acetylsalicylic acid (ASA). 10% ethanol and 50 mg ASA/kg b. wt. were tolerated well. The mucosal lesions consisted of coagulation necrosis and hemorrhages, with a disappearance of histamine and serotonin from the mucosal mast cells in and around the lesion.

Animals↗
PubMed1983

Inhibition of gastric acid secretion by intracerebroventricularly administered prostaglandin e2 in anaesthetized rats.

1 The effect of intracerebroventricularly (i.c.v) administered prostaglandin E2 (PGE2) on gastric acid secretion was studied in anaesthetized rats. 2 Intracerebroventricular injections of 1 and 3 micrograms of PGE2 inhibited gastric acid secretion induced by insulin, electrical vagal stimulation and acetylcholine in a dose-dependent manner. 3 Intravenous injections of 1,3 and 10 micrograms of PGE2 had no effect on insulin-stimulated gastric acid output. 4 The results indicate that upon i.c.v. administration PGE2 inhibits gastric acid secretion by acting centrally and not peripherally after leakage from the central nervous system.

Acetylcholine↗
PubMed1983

Central nervous system effects of arachidonic acid, PGE2, PGF2 alpha, PGD2 and PGI2 on gastric secretion in the rat.

The effects of arachidonic acid, prostaglandin E2 (PGE2), PGF2 alpha, PGD2 and PGI2 on gastric secretion (acid, pepsin and volume) after intracerebroventricular administration were investigated in conscious, pylorus-ligated rats. Arachidonic acid 30-1000 micrograms had no effect on gastric secretion. PGE2 3 and 10 micrograms, reduced gastric secretion as measured 1 hour after injection, although the inhibition induced by 3 micrograms disappeared by 2 h. PGF2 alpha 10 and 30 micrograms, inhibited gastric secretion as measured after 1 h, whereas no change was observed in the gastric contents collected 2 h after 10 micrograms of PGF2 alpha. Intramuscular injection of 30 micrograms of PGF2 alpha had no effect on gastric secretion. Intracerebroventricular administration of 1-30 micrograms of PGD2 or PGI2 had no effect on gastric secretion. The results indicate that PGE2 and PGF2 alpha have a potent central antisecretory action in conscious, pylorus-ligated rats, whereas arachidonic acid, PGD2 and PGI2 do not have any central effects on gastric secretion. It is suggested that PGE2 and PGF2 alpha may be involved in the central nervous system control of gastric secretion.

Animals↗
PubMed1983

Interactions between ethanol and acetylsalicylic acid in damaging the rat gastric mucosa.

The interactions between ethanol (EtOH) and acetylsalicylic acid (ASA) in damaging the gastric mucosa were investigated in urethane-anaesthetised rats upon intragastric irrigation. The addition of 5, 10 or 20 mM ASA to 1 and 4 M EtOH instillates strongly aggravated lesion formation in the gastric mucosa and mucosal bleeding. ASA enhanced the back-diffusion of hydrogen ions into the mucosa induced by 1 M EtOH, whereas gastric mucosal blood flow, which is thought to dispose of the back-diffused acid from the mucosa, remained unchanged, thus resulting in an accumulation of acid within the gastric mucosa. ASA did not further enhance the strongly increased back-diffusion of hydrogen ions induced by 4 M EtOH, but it effectively inhibited EtOH-induced stimulation of the gastric mucosal blood flow, thus causing an increase in the ratio between hydrogen ion back-diffusion and gastric mucosal blood flow. The simultaneous presence of EtOH and ASA did not enhance the rates of absorption of each from the instillates. The results indicate that EtOH and ASA have a strong synergistic action in damaging the gastric mucosa in the rat. The mechanism of this interaction may be an increased accumulation of hydrogen ions within the gastric mucosa, resulting in excessive acidification of the mucosal tissue.

Animals↗
PubMed1983

A comparative study on hypotensive and bradycardic effects of some new imidazole derivatives with possible central mechanism of action.

Cardiovascular actions of 4(5)-(2,6-dimethylbenzyl)imidazole (MPV-207) and its three alkyl bridge analogues were investigated in urethane-anaesthetized normotensive rats. Intravenous (i.v.) injections of 0.001-0.1 mg/kg of MPV-207 lowered mean arterial pressure (MAP) and heart rate (HR) in a dose-dependent manner. The compound was effective also upon intracerebroventricular (i.c.v.) administration. The hypotensive effect of i.v. injected MPV-207 (5 micrograms/kg) was attenuated by i.c.v. administered yohimbine (100 micrograms/kg), an alpha 2-adrenoceptor antagonist. MPV-295 having an ethano group between the phenyl and imidazole moieties decreased MAP and HR at i.v. doses of 0.03-3 mg/kg, being active also after i.c.v. injection. Extension of the alkyl bridge to the propano group further decreased the hypotensive and bradycardic activity, and the compound having a butano bridge was practically inactive. The results indicate that the extension of the alkyl bridge between the phenyl and imidazole rings reduces the hypotensive and bradycardic activities of the MPV compounds. Furthermore, the hypotensive action of these compounds may be mediated by a central mechanism involving a stimulation of alpha-adrenoceptors.

Animals↗
PubMed1982

Gastric mucosal oxidation of ethanol is not involved in ethanol-induced mucosal damage.

The involvement of gastric mucosal metabolism of ethanol in ethanol-induced mucosal damage was studied in urethane anaesthetised rats. Pyrazole, an inhibitor of alcohol dehydrogenase (ADH), slightly aggravated the mucosal lesions produced by intragastric instillation of 30% (v/v) ethanol, but had no effect on increased mucosal permeability to ions, pepsinogen and fluid output or on gastric mucosal blood flow associated with mucosal injury. Induction of ADH by ethanol pre-treatment had no effect on the above-mentioned parameters. Intragastric instillation of acetaldehyde, the product of ethanol oxidation, did not cause lesions in the gastric mucosa. The results suggest that the gastric mucosal toxicity of ethanol may not be related to its metabolism in the gastric mucosa.

Acetaldehyde↗